ライフサイエンスコーパス: atherosclerotic

1 r receptor (LXR) agonists are promising anti-atherosclerotic agents that increase the expression of c

2 reduces the MDA- and IsoLG-lysyl content in atherosclerotic aortas versus 4-HOBA.

3 aive T cells are present in both healthy and atherosclerotic aortas.

4 nent and separate immune cell populations in atherosclerotic aortas.

5 GRNs in the atherosclerotic arterial wall (n = 7) and subcutaneous o

6 ons of human atherosclerotic lesions and non-atherosclerotic arteries were immunostained for CARD8 pr

7 aorta before lesion formation, and in human atherosclerotic arteries when compared with normal arter

8 the two TSP4 variants were assessed in human atherosclerotic arteries.

9 ed directly by autoradiography of normal and atherosclerotic arteries.

10 te in systemic and local immune responses in atherosclerotic arteries.

11 the role of a newly identified regulator of atherosclerotic burden in miR-144 knockout mice receivin

12 n was independently associated with a higher atherosclerotic burden with 3-dimensional vascular ultra

13 blocked SMC transition to SEM cells, reduced atherosclerotic burden, and promoted fibrous cap stabili

14 a_circ_0001445 were proportional to coronary atherosclerotic burden, even after comprehensive adjustm

15 In a cohort of elderly patients with a high atherosclerotic burden, family history of AF is evident

16 new way to regress plaques and alleviate the atherosclerotic burden.

17 de (TMAO), has been associated with coronary atherosclerotic burden.

18 d patients with type 2 diabetes mellitus and atherosclerotic cardiovascular (CV) disease to once-dail

19 iency virus (PLHIV) are at increased risk of atherosclerotic cardiovascular disease (ASCVD) and are p

20 and joint associations of Lp(a) and FHx with atherosclerotic cardiovascular disease (ASCVD) and CHD a

21 Coronary artery calcium (CAC) predicts atherosclerotic cardiovascular disease (ASCVD) events, i

22 statin lipid-modifying medications to reduce atherosclerotic cardiovascular disease (ASCVD) events.

23 (PAD) is associated with increased risk for atherosclerotic cardiovascular disease (ASCVD) events.

24 ing statin therapy for primary prevention of atherosclerotic cardiovascular disease (ASCVD) in adults

25 ults 40 to 70 years of age who are at higher atherosclerotic cardiovascular disease (ASCVD) risk but

26 Estimated 10-year atherosclerotic cardiovascular disease (ASCVD) risk in d

27 on cognition, we examined the ability of the Atherosclerotic Cardiovascular Disease (ASCVD) risk scor

28 Risk of incident atherosclerotic cardiovascular disease (ASCVD), heart fa

29 deficiency virus (PWH) demonstrate increased atherosclerotic cardiovascular disease (ASCVD).

30 erol (LDL-C) and increased risk of premature atherosclerotic cardiovascular disease (ASCVD).

31 taking statins for the primary prevention of atherosclerotic cardiovascular disease (ASCVD).

32 nherited disorders associated with premature atherosclerotic cardiovascular disease (ASCVD).

33 ew paradigm linking aging, inflammation, and atherosclerotic cardiovascular disease (ASCVD).

34 d systemic lupus erythematosus predispose to atherosclerotic cardiovascular disease (ASCVD).

35 s of zero are associated with a low risk for atherosclerotic cardiovascular disease (ASCVD).

36 ) and the presence or absence of established atherosclerotic cardiovascular disease (cardiorenal outc

37 ellitus (T1DM and T2DM) increase the risk of atherosclerotic cardiovascular disease (CVD), resulting

38 e 1 and type 2 diabetes increase the risk of atherosclerotic cardiovascular disease (CVD).

39 and in patients with and without history of atherosclerotic cardiovascular disease (CVD).

40 day was associated with a 14% lower risk of atherosclerotic cardiovascular disease (HR 0.86, 95% CI

41 Similarly, presence of atherosclerotic cardiovascular disease (HR, 0.83 [95% CI

42 versus placebo in patients with established atherosclerotic cardiovascular disease (median follow-up

43 ellitus and either multiple risk factors for atherosclerotic cardiovascular disease (n=10 186) or kno

44 c cardiovascular disease (n=10 186) or known atherosclerotic cardiovascular disease (n=6974).

45 We enrolled patients with atherosclerotic cardiovascular disease (ORION-10 trial)

46 ed with lower risk of heart failure (HF) and atherosclerotic cardiovascular disease among patients wi

47 data for eGFR); 6974 (40.6%) had established atherosclerotic cardiovascular disease and 10 186 (59.4%

48 ebo-controlled trial involving patients with atherosclerotic cardiovascular disease and low-density l

49 blish essential roles for Tregs in resolving atherosclerotic cardiovascular disease and provide mecha

50 wering strategies in high-risk patients with atherosclerotic cardiovascular disease and supports the

51 similar benefit in patients with and without atherosclerotic cardiovascular disease and with and with

52 The individual-level risk of atherosclerotic cardiovascular disease events in primary

53 dose of aspirin for secondary prevention of atherosclerotic cardiovascular disease events.

54 We studied 14 298 patients with atherosclerotic cardiovascular disease from the FOURIER

55 as paradigms for the prevention of premature atherosclerotic cardiovascular disease in all at-risk pa

56 ith current care for secondary prevention of atherosclerotic cardiovascular disease in China, India,

57 An individual's susceptibility to atherosclerotic cardiovascular disease is influenced by

58 r disease (ORION-10 trial) and patients with atherosclerotic cardiovascular disease or an atheroscler

59 terol (HDL-C) level on the expected rates of atherosclerotic cardiovascular disease over the succeedi

60 Aspirin for primary atherosclerotic cardiovascular disease prevention as bas

61 d-lowering recommendations for prevention of atherosclerotic cardiovascular disease rely principally

62 atherosclerotic cardiovascular disease or an atherosclerotic cardiovascular disease risk equivalent (

63 Substantial reduction in expected atherosclerotic cardiovascular disease risk in the next

64 HDL-P for MI by Black ethnicity suggest that atherosclerotic cardiovascular disease risk may differ b

65 ompared to coronary artery calcium score and atherosclerotic cardiovascular disease risk score for MA

66 Atherosclerotic cardiovascular disease risk score, coron

67 s, potential reductions in predicted 30-year atherosclerotic cardiovascular disease risk were greater

68 s with or without metformin in those at high atherosclerotic cardiovascular disease risk.

69 ther refine the assessment and management of atherosclerotic cardiovascular disease risk.

70 th type 2 diabetes mellitus without clinical atherosclerotic cardiovascular disease to guide the use

71 y assigned patients with type 2 diabetes and atherosclerotic cardiovascular disease to receive 5 mg o

72 e considered preoperatively in patients with atherosclerotic cardiovascular disease undergoing vascul

73 y adults >=18 years of age with a history of atherosclerotic cardiovascular disease without safety co

74 culating cystathionine levels are related to atherosclerotic cardiovascular disease, a leading cause

75 ong adults aged 30-84 years with established atherosclerotic cardiovascular disease, adoption of the

76 reatment not only for patients with T2DM and atherosclerotic cardiovascular disease, but also in thos

77 ases, including type 2 diabetes mellitus and atherosclerotic cardiovascular disease, but remain to be

78 Among patients with type 2 diabetes and atherosclerotic cardiovascular disease, ertugliflozin wa

79 ed, controlled trial involving patients with atherosclerotic cardiovascular disease, heterozygous fam

80 n patients with type 2 diabetes mellitus and atherosclerotic cardiovascular disease, in comparison wi

81 ry disease (PAD), the third leading cause of atherosclerotic cardiovascular disease, is undetermined.

82 type 2 diabetes with and without established atherosclerotic cardiovascular disease, most of whom had

83 ess of the patient's previous history of AF, atherosclerotic cardiovascular disease, or HF.

84 Despite all patients having atherosclerotic cardiovascular disease, patients in EMPA

85 with moderate-high future risk of developing atherosclerotic cardiovascular disease, the efficacy and

86 e the inverse relationship between HDL-P and atherosclerotic cardiovascular disease, whereas adjustme

87 of the consistent data for benefit for both atherosclerotic cardiovascular disease- and HF-related o

88 th growing knowledge of the genetic basis of atherosclerotic cardiovascular disease-in particular, co

89 its potential as a therapeutic approach for atherosclerotic cardiovascular disease.

90 therapeutic targeting of SMC transitions in atherosclerotic cardiovascular disease.

91 and advancing age is a major risk factor for atherosclerotic cardiovascular disease.

92 olesterol and an increased risk of premature atherosclerotic cardiovascular disease.

93 atopoiesis associates with increased risk of atherosclerotic cardiovascular disease.

94 l of 'Trojan horse' nanoparticles to prevent atherosclerotic cardiovascular disease.

95 ed with hypolipidemia and protection against atherosclerotic cardiovascular disease.

96 vonoid intake and hospital admissions due to atherosclerotic cardiovascular disease.

97 outcomes mainly in patients with established atherosclerotic cardiovascular disease.

98 diabetes and risk factors for or established atherosclerotic cardiovascular disease.

99 t seem confined to patients with established atherosclerotic cardiovascular disease.

100 so associated with a doubling of the risk of atherosclerotic cardiovascular disease.

101 4 large population studies without baseline atherosclerotic cardiovascular disease: DHS (Dallas Hear

102 of all apoB-containing lipoproteins causing atherosclerotic cardiovascular disease; however, it is u

103 The primary outcome was a composite of atherosclerotic cardiovascular events (myocardial infarc

104 cal strategies aimed at reducing the risk of atherosclerotic cardiovascular events and their adverse

105 ether exposure to an ICI was associated with atherosclerotic cardiovascular events in 2842 patients a

106 gies for primary and secondary prevention of atherosclerotic cardiovascular events in patients with C

107 As such, they are more prone to atherosclerotic cardiovascular events than patients with

108 g or worsening chronic kidney disease and/or atherosclerotic cardiovascular events, and the risk of d

109 techniques in individuals with intermediate atherosclerotic cardiovascular risk according to standar

110 s coronary artery dissection (SCAD) is a non-atherosclerotic cause of myocardial infarction (MI), typ

111 In this Review, we discuss five non-atherosclerotic causes of ACS, including spontaneous cor

112 ice as systemic drugs in the acute phases of atherosclerotic complications favor the healing of wound

113 and TET1 in endothelial cells (ECs) of human atherosclerotic coronary arteries.

114 2 [95% CI: 1.09-3.02]) and (2) lower risk of atherosclerotic coronary artery disease and MI in the UK

115 patients without traditional risk factors of atherosclerotic coronary artery disease.

116 y selective for hydroxyapatite deposition in atherosclerotic coronary plaque.

117 infarction and fatal CHD), ischemic stroke, atherosclerotic CVD (CHD and stroke), heart failure hosp

118 ividuals, a significantly larger number than atherosclerotic CVD (n = 267) and SCORE (Systematic Coro

119 , heart failure hospitalization, global CVD (atherosclerotic CVD and heart failure), and all-cause mo

120 onic kidney disease, and high risk of future atherosclerotic CVD as determined by risk prediction cal

121 rdiology/American Heart Association (10-year atherosclerotic CVD event risk, 5% to < 20%), CAC scorin

122 This Review summarizes the evidence for atherosclerotic CVD in patients with RA and provides a c

123 ssociated with an increased risk of incident atherosclerotic CVD in women.

124 The main aim is to provide a roadmap of atherosclerotic CVD risk management and prevention for p

125 quations and the Pooled Cohort equations for atherosclerotic CVD within five years in a contemporary

126 In patients with atherosclerotic CVD, leukocytes have a hyperinflammatory

127 ith RA have approximately double the risk of atherosclerotic CVD, stroke, heart failure and atrial fi

128 ol) as a causal factor in the development of atherosclerotic CVD.

129 ted as a potential contributor towards human atherosclerotic development.

130 Intracranial atherosclerotic disease (ICAD) is a common cause of stro

131 The degradative SMC phenotype also worsens atherosclerotic disease and could thus be considered as

132 are effective in slowing the progression of atherosclerotic disease and in reducing the risk of thro

133 unclear whether the high risk is due to high atherosclerotic disease burden or if presence of stenosi

134 expression and activity are associated with atherosclerotic disease in patients with chronic kidney

135 isms driving sex as a biological variable in atherosclerotic disease is critical to future precision

136 els alone do not fully reflect the amount of atherosclerotic disease present.(C) RSNA, 2020See also t

137 Fap (Fap(-/-)) in Apoe(-/-) mice accelerated atherosclerotic disease progression in both males and fe

138 treating acute injuries, as well as chronic atherosclerotic disease.

139 es in shaping the development and outcome of atherosclerotic disease.

140 ajor risk modifiers of neurodegenerative and atherosclerotic diseases(1-3), but their effect on cance

141 n outcomes in heart failure patients without atherosclerotic diseases, indicating the importance of i

142 oss of cognitive function might be driven by atherosclerotic effects associated with altered lipid pa

143 tic, anti-inflammatory, anti-tumor, and anti-atherosclerotic effects.

144 We further incubated human atherosclerotic endarterectomy specimens with clinically

145 rs, statins lower the relative risk of major atherosclerotic events by about 22% per 38.7 mg/dl (1 mm

146 (PCSK9) inhibitors, which both reduce major atherosclerotic events in proportion to their effects on

147 etabolic profile and to significantly reduce atherosclerotic events, hospitalization for heart failur

148 est in the use of anticoagulation to prevent atherosclerotic events.

149 whether Tregs are required for resolution of atherosclerotic inflammation and plaque regression, Treg

150 the pathways that mediate the resolution of atherosclerotic inflammation and reversal of plaques are

151 ated the roles of Tregs in the resolution of atherosclerotic inflammation, tissue remodeling, and pla

152 Atherosclerotic Ldlr(-/-) mice were investigated by high

153 lationship between vascular risk factors and atherosclerotic lesion burden of intracranial arteries a

154 r pathway is active in modulated SMCs in the atherosclerotic lesion cap.

155 y, deletion of hematopoietic CARD9 increased atherosclerotic lesion formation and lesion severity.

156 MAARS knockdown reduces atherosclerotic lesion formation by 52% in LDLR(-/-) mic

157 nd that exacerbated dyslipidemia may mediate atherosclerotic lesion formation caused by constant ligh

158 ipopolysaccharide treatment rapidly enhanced atherosclerotic lesion size by expansion of the lesional

159 Neither diabetes nor MI led to increased atherosclerotic lesion size, but diabetes accelerated le

160 er, exogenous TWEAK administration increased atherosclerotic lesion size, lipids, and macrophages con

161 rrowing of coronary lumen space caused by an atherosclerotic lesion.

162 Sections of human atherosclerotic lesions and non-atherosclerotic arteries

163 imaging system to identify the locations of atherosclerotic lesions and occlusion due to myocardial-

164 sms of the formation of clinically dangerous atherosclerotic lesions and the potential of pro-resolvi

165 Atherosclerotic lesions are known for their cellular het

166 Finally, aortic atherosclerotic lesions are reduced by 90% and 70%, resp

167 ine, a specific by-product of MPO, in aortic atherosclerotic lesions as determined by both immunohist

168 lEVs accumulated in plaque atherosclerotic lesions depending on the progression of

169 erived cells within advanced mouse and human atherosclerotic lesions exhibit far greater phenotypic p

170 Atherosclerotic lesions exhibited inflammatory cells.

171 RIPK1 expression is abundant in early-stage atherosclerotic lesions in both humans and mice.

172 , however, an integrated omics assessment of atherosclerotic lesions in individual Apoe(-/-) mice has

173 nce of MPO expression in the bone marrow and atherosclerotic lesions of the aorta in the CKD-bMPOKO m

174 17a1 x Apoe double KO XY mice developed more atherosclerotic lesions than Apoe KO male controls, rega

175 led to an approximately fourfold increase in atherosclerotic lesions throughout the aorta, which were

176 s correlated to mediators of inflammation in atherosclerotic lesions using Biobank of Karolinska Enda

177 several independent human cohorts comparing atherosclerotic lesions versus healthy arteries, using t

178 Human atherosclerotic lesions were enriched in lEVs expressing

179 Rupture and erosion of advanced atherosclerotic lesions with a resultant myocardial infa

180 and association between CVD risk factors and atherosclerotic lesions with LTL.

181 quencing from murine microdissected advanced atherosclerotic lesions with smooth muscle cell (SMC) an

182 ion of macrophages and their accumulation in atherosclerotic lesions without changing the size of les

183 PK1 protein and mRNA in both human and mouse atherosclerotic lesions, and used loss-of-function appro

184 In atherosclerotic lesions, apoA-I exhibits marked oxidativ

185 nction of many cells that make up late-stage atherosclerotic lesions, as well as the mechanisms by wh

186 esolution of inflammation and development of atherosclerotic lesions, but the effects of the P387 TSP

187 the high levels of RIPK1 expression in human atherosclerotic lesions, our study suggests RIPK1 as a f

188 ines and chemokines in endothelial cells and atherosclerotic lesions, suggesting that CARD8 plays a s

189 via reduction of macrophage recruitment into atherosclerotic lesions.

190 g VSMC-specific Aadac showed amelioration of atherosclerotic lesions.

191 regulates the site-specific distribution of atherosclerotic lesions.

192 SGLT2i have moderate benefits on atherosclerotic major adverse cardiovascular events that

193 strategies and prognostic data for these non-atherosclerotic mechanisms of ACS are reviewed.

194 Here we report that SCAD-related MI and atherosclerotic MI exist at opposite ends of a genetic r

195 results: synthetic peptides administered to atherosclerotic mice as systemic drugs in the acute phas

196 e depleted using CD25 monoclonal antibody in atherosclerotic mice during apolipoprotein B antisense o

197 The aortic CD4(+) and T(H1) cell content of atherosclerotic mice that lack MCs was reduced as compar

198 L using cells expressing FR-beta, we studied atherosclerotic mice with (68)Ga-FOL and (18)F-FDG PET/C

199 Using our nanotracer in atherosclerotic mice with myocardial infarction, we obse

200 nvasive imaging biomarker of active coronary atherosclerotic mineralisation.

201 The diverse leukocyte infiltrate in atherosclerotic mouse aortas was recently analyzed in 9

202 Most arterial thrombotic events have a clear atherosclerotic or cardioembolic etiology, but hematolog

203 can mimic arterial dissection, non-calcified atherosclerotic plaque and intraluminal thrombus.

204 ia, coronary artery calcification (CAC), and atherosclerotic plaque are risk factors for the developm

205 beyond its association with total calcified atherosclerotic plaque burden as assessed by coronary ar

206 CT (IVOCT) images, we developed an automated atherosclerotic plaque characterization method that used

207 prevent the deleterious effects of TWEAK on atherosclerotic plaque development and progression.

208 ct4 serves a critical protective role during atherosclerotic plaque development by promoting smooth m

209 nflammatory, oxidized lipids associated with atherosclerotic plaque development.

210 Enhancement of atherosclerotic plaque formation and increase in macroph

211 In summary, eosinophils contribute to atherosclerotic plaque formation and thrombosis through

212 The mechanisms underlying early atherosclerotic plaque formation are not completely unde

213 in enhanced adipose-tissue inflammation and atherosclerotic plaque formation in a mouse model of obe

214 with oxPAPC-driven metabolic changes reduce atherosclerotic plaque formation in mice, thereby unders

215 bone marrow from Abca1(BSM) mice had reduced atherosclerotic plaque formation, similar to mice transp

216 aortic root which are highly susceptible to atherosclerotic plaque formation.

217 ogenesis, cardiorenal fibrosis and increased atherosclerotic plaque formation.

218 lete thrombotic occlusion developing from an atherosclerotic plaque in an epicardial coronary vessel

219 A characteristic feature of the atherosclerotic plaque is the accumulation of apoptotic

220 In atherosclerotic plaque macrophages, ACAT promotes choles

221 der arterial flow conditions on collagen and atherosclerotic plaque material, were attenuated by riva

222 The main outcomes were newly diagnosed atherosclerotic plaque on carotid bifurcation or interna

223 is association between ICI use and increased atherosclerotic plaque progression was attenuated with c

224 , in an imaging substudy (n=40), the rate of atherosclerotic plaque progression was compared from bef

225 involved in the thrombus formation stage on atherosclerotic plaque rupture, we hypothesized that fac

226 ies, and, in a hyperlipidemia model, reduced atherosclerotic plaque size while increasing markers of

227 ur findings identify HDAC9 as a regulator of atherosclerotic plaque stability and IKK activation thus

228 cells and expression of CX3CL1 and LFA-3 in atherosclerotic plaque tissues from HIV-uninfected donor

229 n are interrelated processes contributing to atherosclerotic plaque vulnerability.

230 y response and deposits in foam cells at the atherosclerotic plaque, it also regulates cellular mecha

231 alled carbon nanotubes accumulate within the atherosclerotic plaque, reactivate lesional phagocytosis

232 tive CD4(+) T-helper cells accumulate in the atherosclerotic plaque.

233 phy angiography can characterize subtypes of atherosclerotic plaque.

234 ncreased (18)F-fluoride activity in coronary atherosclerotic plaque.

235 ro-inflammatory myeloid cells accumulated in atherosclerotic plaques and at the myocardial infarct si

236 nscriptome-based cellular landscape of human atherosclerotic plaques and highlights cellular plastici

237 lement system is a major alteration in early atherosclerotic plaques and is reflected by increased C5

238 represent a major immune cell population in atherosclerotic plaques and play central role in the pro

239 Non-invasively detecting atherosclerotic plaques and stenosis using NETs may lay

240 coronary artery ligation to mimic vulnerable atherosclerotic plaques and their rupture leading to MI.

241 hod generates complete 3D reconstructions of atherosclerotic plaques and uncovers their volume, geome

242 number and activity of T cell subsets in the atherosclerotic plaques are critical for the prognosis o

243 Microcalcifications in atherosclerotic plaques are destabilizing, predict adver

244 we demonstrated PCSK6 upregulation in human atherosclerotic plaques associated with smooth muscle ce

245 in VSMCs in thin fibrous caps of late-stage atherosclerotic plaques compared to early fibroatheroma

246 viously reported to be up-regulated in human atherosclerotic plaques compared with normal vessel.

247 Dogma suggests that atherosclerotic plaques expand primarily via the accumul

248 Atherosclerotic plaques from HFD-treated KO mice showed

249 led accumulation of the nanoparticles in the atherosclerotic plaques increased by 3.3-fold following

250 n PET-positive, CT-negative regions of human atherosclerotic plaques is the result of developing micr

251 nd in primary human coronary artery SMCs and atherosclerotic plaques obtained at carotid endarterecto

252 herosclerosis, which was also found in human atherosclerotic plaques of carotid and coronary arteries

253 phils and in the inflammatory environment of atherosclerotic plaques of diabetic mice after cholester

254 LOX-1 NTFs, develop larger and more advanced atherosclerotic plaques than controls.

255 single-cell ATAC sequencing on human carotid atherosclerotic plaques to define the cells at play and

256 rcted myocardium, inflamed lung regions, and atherosclerotic plaques using a clinical PET/magnetic re

257 ports showing the presence of enterovirus in atherosclerotic plaques we hypothesized that the coxsack

258 and numbers of CD68-positive macrophages in atherosclerotic plaques were lower in Flna-deficient mic

259 markedly reduced in VSMCs in human and mouse atherosclerotic plaques, and in human VSMCs derived from

260 In vivo-administered msR4M-L1 enriches in atherosclerotic plaques, blocks arterial leukocyte adhes

261 tokines, which are present at high levels in atherosclerotic plaques, play important roles in regulat

262 valence of coronary artery calcification and atherosclerotic plaques, which are strong predictors for

263 d epigenetic heterogeneity of macrophages in atherosclerotic plaques.

264 ivated in inflammatory macrophages and human atherosclerotic plaques.

265 s and that necroptosis is active in advanced atherosclerotic plaques.

266 CD4(+) T cells are commonly found in atherosclerotic plaques.

267 s-affine Gadofluorine P for molecular MRI of atherosclerotic plaques.

268 esterol transport, resulting in reduction of atherosclerotic plaques.

269 f atherosclerosis but are seldom detected in atherosclerotic plaques.

270 reduced plasma total cholesterol levels and atherosclerotic plaques.

271 phages are the most abundant immune cells in atherosclerotic plaques.

272 scular events are often caused by rupture of atherosclerotic plaques.

273 -cell RNA sequencing of both mouse and human atherosclerotic plaques.

274 a promising therapeutic target to stabilize atherosclerotic plaques.

275 tes, suggesting a more benign composition of atherosclerotic plaques.

276 for imaging of smooth muscle cells (SMCs) in atherosclerotic plaques.

277 are capable of Ag presentation within human atherosclerotic plaques.

278 igher in advanced than in intermediate human atherosclerotic plaques.

279 clerosis and the process of T cell homing to atherosclerotic plaques.

280 ocalized with Mac-3-positive macrophage-rich atherosclerotic plaques.

281 ersity of cells present in tissues including atherosclerotic plaques.

282 chanism by which enterovirus infect cells in atherosclerotic plaques.

283 th an acute coronary syndrome (ACS), but non-atherosclerotic processes are also important contributor

284 pression of MAARS increases by 270-fold with atherosclerotic progression and decreases with regressio

285 on of IP3R1 in epsin-deficient mice restores atherosclerotic progression.

286 lly once to WT (wild type) or once weekly to atherosclerotic prone mice.

287 m cell formation compared to standard DES in atherosclerotic rabbits.

288 Elevated genetic risk was additive to major atherosclerotic risk factors and identified patients mor

289 Patients were also categorized by major atherosclerotic risk factors including diabetes mellitus

290 ed using 9,710 participants (19% black) from Atherosclerotic Risk in Communities (ARIC) (enrolled 198

291 promising non-invasive approach for refined atherosclerotic risk prediction.

292 cholesterol content is hypothesized to drive atherosclerotic risk.

293 mong steatosis and atherosclerosis, specific atherosclerotic sites, multiple-site atherosclerosis, an

294 s in 2860 patients with ischemic stroke with atherosclerotic stenosis of cerebral vasculature.

295 tionships between NT-proBNP and large-artery atherosclerotic stroke, IGFBP3 and diabetes mellitus as

296 modulation of smooth muscle cells (SMCs) in atherosclerotic tissues and promotes a fibroblast phenot

297 -related SMC-to-chondromyocyte transition in atherosclerotic tissues.

298 yndrome or atrial fibrillation trial (versus atherosclerotic vascular disease or diabetes mellitus/pr

299 , SiglecF(hi) neutrophils were also found in atherosclerotic vessels, revealing that they arise acros

300 It has been suggested that miR-144 is pro-atherosclerotic via effects on reverse cholesterol trans